Abstract

Aim: To determine the role of fetuin-A, a glycoprotein which represents the alpha-2 band of protein electrophoresis and which prevents the precipitation of calcium both in the intravascular and extravascular areas, in the etiology of urolithiasis. Material and Method: Sixty-nine patients (55 patients with urolithiasis and 14 patients with a history of urolithiasis) and 44 control subjects (patients without urolithiasis) were included in the study. Fetuin-A concentrations were measured by the enzyme-linked immunosorbent assay method both in the serum and in 24-hour urine samples obtained from the patients and the control group. In addition, the other activators and inhibitors that may play a role in urolithiasis were measured biochemically. Results: There were no statistically significant differences in serum sodium, potassium, creatinine, calcium, magnesium, phosphorus, uric acid, albumin, and parathyroid hormone levels between the patients and the control group. Daily urine volume, magnesium, uric acid, potassium, sodium, calcium, phosphorus, citrate, oxalate and cystine levels measured in 24-hour urine collections were similar in both the patients and the control groups. The serum fetuin-A level was 0.5 g/l in the patients with urolithiasis, 0.45 g/l in the patients with a history of urolithiasis, and 0.51 g/l in the control group (p > 0.05). The urine fetuin-A levels were 8.71, 5.7 and 10.81 mg/d, respectively (p > 0.05). The data were not statistically significant between the 3 groups. Conclusion: There was no difference in between the serum and urine fetuin-A levels between the groups with and without urolithiasis. This result does not correlate with the results of another study which suggested a role for fetuin-A in the etiology of urolithiasis. This discrepancy needs to be elucidated with a larger population in further studies.

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